Until recently, the precise nature of hypothalamic control over vagal neurons controlling gastric motility, bloodflow and secretion was a matter for speculation. This was due largely to the fact that hypothalamic lesions and stimulation (the predominant means of study) produced equivocal gastrointestinal effects. Recent advances in neuroanatomical tracing techniques have revealed that only one direct hypothalamo-vagal motor projection exists. This projection is derived entirely from the paraventricular nucleus of the hypothalamus. The experiments presented herein will begin the physiologic and pharmacologic description of this projecting by utilizing advanced neurophysiological methods coupled with classical measures of gastric function. In particular, we will apply single-neuron recording techniques to physiologically identified gastric vagal neurons and paraventricular hypothalamic neurons. By using microstimulation and spike-triggered averaging methods the nature of the direct hypothalamic-gastric vagal projection will be estimated. Next, we will microiontophorese putative peptide neuro-effectors onto identified gastric vagal neurons in an attempt to mimic the effects of paraventricular hypothalamic input upon these parasympathetic preganglionic neurons. Finally, the physiological significance of these observations will be tested by repeating them while recording indices of gastric acid production and gastric motility. The objective of this and succeeding studies is the unequivocal elucidation of the nature of direct hypothalamic projections upon parasympathetic preganglionic neurons which regulate gastric function. Given that a variety of stress-induced gastrointestinal pathology, particularly ulcers, may be neurogenic in origin, the results of these studies may demonstrate the way in which the hypothalamus might be directly involved in the production of such pathology.